@phdthesis{oai:mie-u.repo.nii.ac.jp:00012791,
 author = {Yamamoto, Wakako and 山本, 和歌子},
 month = {Mar},
 note = {application/pdf, B-1a cells are distinguishable from conventional B cells, which are designated B-2 cells, on the basis of their developmental origin, surface marker expression, and functions. In addition to the unique expression of the CD5 antigen, B-1a cells are characterized by the expression level of CD23. Although B-1a cells are considered to be independent of T cells and produce natural autoantibodies that induce the clinical manifestations of autoimmune diseases, there is much debate on the role of B-1a cells in the development of autoimmune diseases. We examined the involvement of B-1a cells in autoimmune-prone mice with the lpr gene. MRL/lpr and B6/lpr mice exhibited lupus and lymphoproliferative syndromes because of the massive accumulation of CD3+CD4-CD8-B220+ T cells. Interestingly, B220+CD23-CD5+ (B-1a) cell population in the peripheral blood and peritoneal cavity increased with age and disease progression. Ninety percent of B-1a cells were CD3 positive (CD3+ B-1a cells) and did not produce tumor necrosis factor alpha, interfer on gamma, or interleukin-10. To test the possible involvement of CD3+ B-1a cells in autoimmune disease, we tried to eliminate the peripheral cells by hypotonic shock through repeated intraperitoneal injections of distilled water. The fraction of peritoneal CD3+ B-1a cells decreased, and symptoms of the autoimmune disease were much milder in the distilled water-treated MRL/lpr mice. These results suggest CD3+ B-1a cells could be mediators of disease progression in autoimmune-prone mice., 本文/Department of Pediatrics, Mie University Graduate School of Medicine, 2-174 Edobashi Tsu Mie, Japan 514-8507, 19p},
 school = {三重大学},
 title = {CD3+ B-1a cells as a mediator of disease progression in autoimmune prone mice},
 year = {2019},
 yomi = {ヤマモト, ワカコ}
}